Biomedical Research

Neurons exposed to Aβ will be apoptotic in Alzheimer's disease (AD) brains or in vitro. The aim of the current study is to explore the neuroprotective mechanism that 7,8-dithydroxycoumarin inhibits JNK and p38MAPK-mediated Aβ-induced neurotoxicity. In vitro cultures of SH-SY5Y human neuroblastoma cell lines were treated with 7,8-dithydroxycoumarin (0, 1, 5 and 10 μmol/L) for 1.5 h, subsequently treated with 25 μmol/L Aβ25-35 fibrils. The MTT method was used to detect cell proliferation, and fluorescence probe H2DCF-DA was used to determine intracellular reactive oxygen species (ROS) content. Western-blot assay was performed to detect the JNK and P38MAPK phosphorylation. 25 μmol/L Aβ25-35 fibrils suppressed cell growth. They increased intracellular ROS, and enhanced levels of JNK and P38MAPK phosphorylation in a time-dependent manner. 7,8-dithydroxycoumarin treatment improved cell proliferation, reduced ROS generation and down-regulated levels of JNK and p38MAPK phosphorylation in a concentration-dependent manner. 7,8-dithydroxycoumarin may inhibit Aβ-induced neurotoxic injury through suppressing ROS, JNK and p38MAPK pathways. The finding of the current study is conducive to protecting neurons in AD by using 7,8-dithydroxycoumarin.